Primary immunodeficiencies of the B lymphocyte.

The immune response consists of two main components: humoral immunity represented by B lymphocytes and cellular immunity maintained by the T lymphocytes. Immunoglobulins, produced by B-lymphocytes, are the main mediators of humoral immunity, and deficiencies at this level affect the body's response to infection. Plasmocytes produce nine antibody izotypes: immunoglobulins G (IgG1, IgG2, IgG3, IgG4), immunoglobulins M (IgM), immunoglobulins A (IgA1, IgA2), immunoglobulins D (IGD) and immunoglobulins E (IgE). Primary hypogammaglobulinemias are characterized by the occurrence of recurrent infections and, paradoxically, by the occurrence of autoimmune diseases. Characteristic for these diseases is that symptoms occur at 7-9 months after birth, when transplacental antibody titers transmitted from the mother decrease, and the infant's body is unable to synthesize them to normal levels. Primary hypogammaglobulinemias are transmitted genetically, but mutations at the molecular level are still not fully understood. The most common are: Bruton agammaglobulinemia, transient newborn hypogammaglobulinemia, selective immunoglobulin deficiency and variable common immunodeficiency. Treatment consists of monthly antibiotics and immunoglobulins, depending on antibody titers (except for IgA deficiency).

Cytotoxic antibodies--valuable prognostic factor for long term kidney allograft survival.

BACKGROUND: Since the first attempts of kidney transplant, the inflammation mediated by T lymphocytes was considered one of the most important processes implicated in graft rejection but, multiple acute and chronic graft rejects revealed that the inflammation process is not singular and humoral mechanisms may play a role in the development of chronic vascular rejection. MATERIAL AND METHODS: We evaluated 500 Romanian patients registered on the kidney transplant waiting list. We performed anti-HLA class I and class II antibodies screening and identification. Laboratory tests were performed at Centre for Immunogenetics and Virology, Fundeni Clinical Institute, Bucharest, Romania. The methods used are represented by ELISA (GTI Diagnosis, USA) and Luminex (Tepnel, USA) RESULTS: pretransplant evaluation of the subjects illustrates that 145 patients (29%) have been sensitized and 355 patients (71%) have not been sensitized. The most frequent types of anti-HLA antibodies were A2 (13%), B42 (10%), DR7 and DR11 (13%). Post transplant, the most cases with de novo antibodies were observed in the first 6 months post transplantation. High serum levels of Il-2 Receptor, TNF-alpha and neopterin in post transplant sensitized patients were observed following de novo cytotoxic antibodies occurrence. CONCLUSION: post renal transplantation, patients present high risk in developing de novo cytotoxic antibodies, especially those who had HLA mismatch with the donor. These antibodies are predictors for acute graft rejection and for graft failure.